Nuclear factor Y (NF-Y) constitutes a pivotal transcription factor family that modulates plant growth and development as well as abiotic stress responses. Oat (Avena sativa L.) is an economically vital cereal crop and a major livestock forage globally. Nevertheless, the NF-Y gene family has not yet been systematically characterized in the oat genome. Here, we identified 36 AsNF-Y genes in the oat genome and categorized them into three distinct subfamilies (NF-YA, NF-YB, and NF-YC). Phylogeny, gene structure, duplication, collinearity, and conserved motif analyses revealed high evolutionary conservation of this gene family. Additionally, the identification of diverse cis-acting regulatory elements in the promoters of AsNF-Y genes, combined with their differential expression profiles under multiple abiotic stress conditions, indicated that AsNF-Ys serve as crucial regulators in modulating oat abiotic stress tolerance. Furthermore, preliminary functional validation via the TRV-VIGS system confirmed that two candidate genes, AsNF-YC02 and AsNF-YC06, may positively regulate salt tolerance in oat. Collectively, our findings deepen the understanding of NF-Y genes in gramineous crops and supply promising candidates for the genetic improvement of oat stress tolerance and molecular breeding.
Cailian Du, Yvkun Xue, Hao Wang et al.· Plants· 0 citations
Chronic exposure to lead (Pb) represents a persistent environmental hazard that can impair hippocampal integrity and cognitive function, while effective protective strategies remain limited. Ginsenoside Rg1 is an important bioactive constituent derived from Panax ginseng and has been reported to possess antioxidant and neuroprotective activities; however, its involvement in Pb-triggered ferroptosis-associated neuronal damage remains unclear. In the present study, a male C57BL/6J mouse model of subchronic lead acetate exposure and a lead-exposed HT22 cell model were established. Behavioral and histopathological changes were assessed, followed by analysis of inflammatory responses, oxidative stress, ferroptosis-related alterations, and Nrf2-associated signaling. Rg1 improved cognitive performance and attenuated hippocampal neuronal loss, neuroinflammatory activation, oxidative injury, and ferroptosis-related alterations, including ferrous ion accumulation and mitochondrial damage. Consistently, Rg1 restored SLC7A11/xCT and GPX4 expression and enhanced Nrf2-associated antioxidant signaling, whereas the Nrf2 inhibitor ML385 weakened the Rg1-induced increases in nuclear Nrf2, NQO1, and GPX4. Collectively, these findings indicate that Rg1 alleviates lead-induced neurotoxicity and support the involvement of Nrf2 signaling in the regulation of oxidative stress and ferroptosis-related injury. These findings provide experimental evidence supporting further preclinical investigation of Rg1 and its Nrf2-associated neuroprotective mechanisms in Pb-induced neuronal injury.
Yiyao Gong, Jie Zhang, Tingting Wang et al.· Molecules· 0 citations
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